High-Intensity Post-Stroke Rehabilitation Is Associated with Lower Risk of Pressure Ulcer Development in Patients with Stroke: Real-World Evidence from a Nationwide, Population-Based Cohort Study.

Background and Objectives: Multiple factors are associated with pressure ulcer (PU) development, including limited mobility following stroke. We performed a nationwide cohort study to investigate the impact of rehabilitation intensity on the incidence of post-stroke PU. Materials and Methods: Data of patients diagnosed with stroke between 2000 and 2012 were collected from the 2000 Longitudinal Health Insurance Database (Taiwan). Based on the number of rehabilitation sessions attended within 90 days of discharge, the rehabilitation intensity was classified as low, medium, or high. After adjusting for sociodemographic factors and comorbidities, the Cox proportional hazards model evaluated the risk of PU development during the 12-year follow-up period. Kaplan−Meier curves were used to estimate the cumulative incidence of PUs. Results: Our study included 18,971 patients who had their first episode of stroke. Of these, 9829 (51.8%) underwent rehabilitation therapy after discharge. Female patients and patients with a National Institutes of Health Stroke Scale (NIHSS) score >13 points, who commenced high-intensity post-stroke rehabilitation after discharge had a significantly lower risk of PU development than those who underwent low-intensity post-stroke rehabilitation after discharge. Cumulative survival analysis showed a significantly lower cumulative incidence of PU during the 12-year follow-up period in the high-intensity rehabilitation group. Conclusion: Compared with low-intensity post-stroke rehabilitation, high-intensity post-stroke rehabilitation after discharge from hospital is associated with a lower risk of post-stroke PU development, especially in female stroke patients and patients with a NIHSS score >13 points. High-intensity rehabilitation is also associated with a significantly lower cumulative incidence of PU events during the 12-year follow-up period.

Brain Magnetic Resonance Imaging of Intracerebral Hemorrhagic Rats after Alcohol Consumption.

BACKGROUND: Alcoholism is one of the risk factors for cerebrovascular diseases. Our previous study demonstrated that acute alcohol intoxication enhances brain injury and neurological impairment in rats suffering from intracerebral hemorrhage (ICH). We plan to investigate the effect of chronic alcohol consumption (CAC) in rats with ICH by magnetic resonance imaging (MRI). METHODS: Sixteen Sprague-Dawley male rats were divided into 2 groups: CAC group (fed with 10% alcohol drinking water for 4 weeks, n = 8), and Control group (plain drinking water, n = 8). ICH was induced by collagenase infusion into the right striata of all rats. Coronal T1-weighted imaging, T2-weighted imaging, T2*-weighted imaging, and diffusion-weighted imaging were generated with a 3.0T MRI scanner to investigate the changes of hemorrhagic volume and edema throughout the injury and recovery stages of ICH in rats. RESULTS: T2-weighted imaging is ideal for monitoring hematoma volume in rats. The hematoma volume was larger in the CAC group than in the control group (P < .001), however, did not correlate to post-ICH progressive edema formation (P > .7), and neurological impairment (P > .28) between the 2 groups, respectively. DISCUSSION: Although our findings indicate that CAC induces larger hematoma in rats with ICH, the underlying mechanism should be studied in the future.

Collagenase-Induced Rat Intra-Striatal Hemorrhage Mimicking Severe Human Intra-Striatal Hemorrhage.

Basal ganglia hemorrhage accounts for approximately 50% of all hemorrhagic strokes. A good rat model that produces severe intrastriatal hemorrhage (ISH) mimicking human severe ISH is lacking. The present study compared the intra-striatal injection of 0.2 U with that of 0.6 U of collagenase in inducing severe ISH in rats. Three-Tesla (3T) magnetic resonance imaging (MRI) was used to evaluate brain injuries in terms of hematoma size (volume), midline shift (MLS), and brain edema. This evaluation was further substantiated by determination of behavior and neurologic functions and mortality over 56 h. The 0.2 U collagenase caused hematoma volume increases for 10.3 to 30.1 mm³, while the 0.6 U caused 36.4 to 114.8 mm³, at post-ISH 1 h to 56 h. The 0.6 U collagenase significantly increased MLS to 1.5-3.0 times greater than the 0.2 U did at all post-intracerebral hemorrhage (ICH) time points. The MLS increased dependently with hematoma expansion with high correlation coefficients, yet no mortality occurred. These two dosages, nevertheless, caused the same pattern and severity in relative apparent diffusion coefficient (rADC) changes for three regions of interest (ROIs). Both ISH models induced consistent behavior deficits. The larger dosage produced severe brain injuries as well as neurological deficits, more closely mimicking severe human ISH. Hematoma volume and MLS can be the most useful parameters for evaluating the ISH severity in the present experimental model. The larger dosage, therefore, would be useful for investigating the pathophysiology of the severer ISH in the striatum. This may be applied for evaluating potential therapeutic strategies and outcomes in the future.

Acute Alcohol Intoxication Aggravates Brain Injury Caused by Intracerebral Hemorrhage in Rats.

OBJECTIVE: Alcohol intoxication is associated with worse intracerebral hemorrhage (ICH) outcome, indicating the important role of alcohol in ICH pathogenesis. We intended to investigate the effects of ethanol pretreatment on the severity of ICH-induced brain injury in rats. METHODS: At 1 hour after intraperitoneal injection of ethanol (3 g/kg), 0.2 U bacterial collagenase was infused into the striatum of male Sprague-Dawley rats to induce ICH. Accumulative mortality rate, body weight changes, and motorsensory and neurological abnormalities were evaluated. The hemorrhagic volume, hematoma expansion, and water content were measured by Drabkin's method, morphometric assay, and dry/wet method, respectively. Blood-brain barrier disruption was assessed using Evans blue assay. Oxidative stress was evaluated by the enzymatic activity of glutathione peroxidase, oxidation of hydroethidine, and the production of malondialdehyde. Cerebral blood flow perfusion volume and hypo-/hyperperfusion neuroimaging were examined by magnetic resonance imaging. RESULTS: Ethanol pretreatment aggravates the hematoma hemolysis, hemorrhagic volume, hematoma expansion, brain edema, blood-brain barrier disruption, microglial activation, elevated oxidative stress, and neuroinflammation in the hemorrhagic striatum. The summation effect of these consequences is the major cause of marked neurological impairment and higher mortality rate (64%) in ethanol-pretreated rats with ICH. CONCLUSION: This is a novel model to evaluate the effects of high-dose alcohol administration on experimental ICH rats. IMPLICATIONS: The present study may provide clues for making novel strategies in the management of patients with ICH who overconsume alcoholic drinks before the attack.

Risk of Incident Stroke among Vegetarians Compared to Nonvegetarians: A Systematic Review and Meta-Analysis of Prospective Cohort Studies.

Vegetarian dietary patterns provide health benefits for cardiovascular health; however, the studies examining the association of vegetarian diets with stroke incidence showed inconsistent findings. We systematically evaluated the risk of incident stroke among vegetarians (diets excluding meat, poultry, fish, and seafood) compared among nonvegetarians. A systematic search of PubMed, EMBASE, Cochrane Library, and Web of Science was performed until 20 May 2021. Prospective cohort studies comparing the risk estimates for incident stroke between vegetarians and nonvegetarians were included. Of 398 articles identified in the database search, data from seven cohort studies (408 total stroke cases in 29,705 vegetarians and 13,026 total stroke cases in 627,728 nonvegetarians) were included. The meta-analysis revealed no significant association between adhering to the vegetarian dietary patterns and the risk of incident stroke (HR = 0.86; 95% CI = 0.67-1.11; I2 = 68%, n = 7). Subgroup analyses suggested that studies conducted in Asia and those with a mean baseline age of participants 50-65 years showed a lower risk of stroke in vegetarians. Moreover, no significant association between vegetarian diets and the risk of ischemic stroke (HR = 0.56; 95% CI = 0.22-1.42; I2 = 82%, n = 3) or hemorrhagic stroke (HR = 0.77; 95% CI = 0.19-3.09; I2 = 85%, n = 2) was found. To be conclusive, no strong relationship between vegetarian diets and the incidence of stroke was observed. Given the limited certainty of evidence from NutriGrade, future well-designed studies are warranted to provide solid evidence on this topic.

Spinal cord stimulation for spinal cord injury patients with paralysis: To regain walking and dignity.

Spinal cord injury (SCI) usually leads to disconnection between traversing neuronal pathway. The impairment of neural circuitry and its ascending and descending pathway usually leave severe SCI patients with both motor disability and loss of sensory function. In addition to poor quality of life, SCI patients not only have disabling respiratory function, urinary retention, impaired sexual function, autonomic dysregulation but also medical refractory neuropathic pain in the long term. Some translational studies demonstrated that spinal networks possess a dynamic state of synaptic connection and excitability that can be facilitated by epidural spinal cord stimulation. In addition, preliminary human studies also confirmed that spinal cord stimulation enables stepping or standing in individuals with paraplegia as well. In this review, we examined the plausible interventional mechanisms underlying the effects of epidural spinal cord stimulation in animal studies. Following the success of translational research, chronic paralyzed subjects due to SCI, defined as motor complete status, regained their voluntary control and function of overground walking and even stepping for some. These progresses lead us into a new hope to help SCI patients to walk and regain their independent life again.

Delayed formation of hematomas with ethanol preconditioning in experimental intracerebral hemorrhage rats.

OBJECTIVE: Spontaneous intracerebral hemorrhage (ICH) accounts for 10%-15% of all strokes and causes high mortality and morbidity. In the previous study, we demonstrated that ethanol could aggravate the severity of brain injury after ICH by increasing neuroinflammation and oxidative stress. In this study, we further investigate the acute effects of ethanol on brain injury within 24 h after ICH. MATERIALS AND METHODS: Totally, 66 male Sprague-Dawley rats were assigned randomly into two groups: saline pretreatment before ICH (saline + ICH), and ethanol pretreatment before ICH (ethanol + ICH). Normal saline (10 mL/kg) or ethanol (3 g/kg, in 10 mL/kg normal saline) was administered intraperitoneally 1 h before induction of experimental ICH. Bacterial collagenase VII-S (0.23 U in 1.0 µL sterile saline) was injected into the right striatum to induce ICH in the rats. We evaluated the hematoma expansion, hemodynamic parameters (heart rate and blood pressure), activated partial thromboplastin time (aPTT), prothrombin time (PT), and striatal matrix metallopeptidase 9 (MMP-9) expressions at 3, 6, 9, and 24 h after ICH. RESULTS: The ethanol + ICH group exhibited decreased hematoma at 3 h after ICH; nevertheless, there was a larger hematoma compared with the saline + ICH group at 9 and 24 h after ICH. The ethanol + ICH group had lower blood pressure at 3, 6, and 9 h post-ICH, but both groups maintained similar heart rates after ICH. There was no significant difference in the aPTT and PT between the two groups. Incremental ethanol concentrations had no influence on collagenase VII-S activity at 120 min in vitro. MMP-9 expression was upregulated in the right striata of the ethanol + ICH group, especially at 3 and 9 h after ICH. CONCLUSION: Ethanol delayed hematoma formation in the first 3 h due to a hypotensive effect; however, the accelerated growth of hematomas after 9 h may be a sequela of ethanol-induced MMP-9 activation.

Thiazide diuretics and the risk of hip fracture after stroke: a population-based propensity-matched cohort study using Taiwan's National Health Insurance Research Database.

OBJECTIVES: This study aimed to investigate the association between thiazide use and the risk of hip fracture after stroke. SETTING: A population-based, propensity-matched cohort study was conducted on the basis of Taiwan's National Health Insurance Research Database. PARTICIPANTS: Patients with newly diagnosed ischaemic stroke between 2000 and 2011 were included. After propensity score matching, 7470 patients were included, of whom 3735 received thiazides and 3735 did not. OUTCOME MEASURES: HRs for developing hip fractures within 2 years after stroke were calculated using Cox proportional hazards regression model with adjustments for sociodemographic and coexisting medical conditions. RESULTS: Overall, patients using thiazides after stroke had a lower risk of hip fracture than those not using thiazides (8.5 vs 13.9 per 1000 person-years, adjusted HR=0.64, 95% CI 0.46 to 0.89, p=0.007). Further sensitivity analysis based on the duration of thiazide use revealed that the risk of hip fracture tended to decrease as the duration of exposure of thiazides increased. However, the effect was significant only in patients with long-term use of thiazides (using thiazides for >365 days within 2 years after stroke), with a 59% reduction in the risk of hip fracture when compared with patients not using thiazide (adjusted HR=0.41, 95% CI 0.22 to 0.79, p=0.008). CONCLUSIONS: The long-term use of thiazides is associated with a decreased risk of hip fracture after stroke.

Post-ischemic stroke rehabilitation is associated with a higher risk of fractures in older women: A population-based cohort study.

BACKGROUND: Rehabilitation can improve physical activity after stroke. However, patients may be more prone to falls and fractures because of balance and gait deficits. Few reports have studied the relationship between rehabilitation and subsequent fractures after ischemic stroke. OBJECTIVE: To investigate whether post-stroke rehabilitation affects fracture risk. METHODS: We conducted a population-based retrospective cohort study based on the Taiwan National Health Insurance Research Database. Patients with a newly diagnosed ischemic stroke between 2000 and 2012 were included. After propensity score matching, a total of 8,384 patients were enrolled. Half of the patients (4,192) received post-stroke rehabilitation within 1 month; the other half did not receive any post-stroke rehabilitation. Cox proportional hazards regression model was used to calculate hazard ratios (HRs) for fractures among patients with and without rehabilitation within 1 year after ischemic stroke. Patients were further stratified by sex and age (20-64 and ≥65 years). RESULTS: Patients receiving post-stroke rehabilitation had a higher incidence of fracture (6.2 per 100 person-years) than those who did not (4.1 per 100 person-years) after adjustment for sociodemographic and coexisting medical conditions [HR = 1.53, 95% confidence interval (CI) = 1.25-1.87, p < 0.001]. The analyses performed after stratifying for sex and age showed that only older women undergoing rehabilitation had a significantly higher risk of fracture (HR = 1.62, 95% CI = 1.21-2.17, p = 0.001). CONCLUSION: Rehabilitation after ischemic stroke is associated with an increased fracture risk in older women.

Sustained-release versus immediate-release glipizide for treatment of type 2 diabetes mellitus in chinese patients: A randomized, double-blind, double-dummy, parallel-group, 12-week clinical study.

BACKGROUND: Few data exist that have compared sulfonylurea formulations in differing ethnic populations. Most studies of sulfonylureas have been performed in white patients with type 2 diabetes mellitus. OBJECTIVE: The aim of this study was to compare the efficacy and tolerability of a sustained-release glipizide (GSR) formulation with those of immediate-release glipizide (GIR) in Chinese patients with type 2 diabetes mellitus. METHODS: This randomized, double-blind, double-dummy, placebo-controlled, parallel-group, clinical study enrolled adult patients with type 2 diabetes mellitus who were already being treated with diet and a sulfonylurea. Patients were randomized to receive either GSR 10 mg PO QD or GIR 5 mg PO BID for 12 weeks. Because these 2 formulations differed in appearance, each patient also received placebo resembling the alternate formulation, to be received at the alternate frequency. Drugs dispensed but not used were returned to the investigators and counted to monitor compliance with the protocol. For efficacy assessment, fasting plasma glucose (FPG) and glycosylated hemoglobin (HbA(1c)) were measured before and after treatment. Tolerability was measured by adverse events (AEs), which were evaluated by the attending physician during each clinical visit. RESULTS: Of the 57 patients (37 men, 20 women) enrolled in the study, 41 completed it. All were Han Chinese of Taiwanese origin, and had the following characteristics: age range, 33 to 69 years; mean (SE) height, 161.99 (9.42) cm; and mean (SE) body mass index, 25.21 (3.43) kg/m2. An intent-to-treat analysis found that the mean (SE) changes from baseline in FPG (-30.00 [10.67] vs -25.96 [11.15] mg/dL) and in HbA(1c) (-0.08% [0.24%] vs +0.14% [0.22%]) during the 12-week period of the study were not significantly different between the 2 formulations. For patients in the per-protocol analysis, mean (SE) changes from baseline in FPG (-30.00 [10.67] vs -16.52 [7.79] mg/dL) and HbA(1c) (-0.08% [0.24%] vs +0.11% [0.25%]) were also not significantly different. The most frequently reported AEs were urinary abnormality (22.2%) and tachycardia (6.7%) for the GSR group and GIR group, respectively. No serious drug-related AEs were observed in either group. CONCLUSION: In this small study, treatment with oral GSR (10 mg QD) was not significantly different from that of treatment with GIR (5 mg BID) with respect to short-term (12 weeks) FPG and HbA(1c) reductions in these ethnic Chinese adults with type 2 diabetes mellitus receiving treatment with a sulfonylurea.